Polyvalent human immunoglobulin for infectious diseases: Potential to circumvent antimicrobial resistance

Abstract

Antimicrobial resistance (AMR) is a global health problem that causes more than 1.27 million deaths annually; therefore, it is urgent to focus efforts on solving or reducing this problem. The major causes of AMR are the misuse of antibiotics and antimicrobials in agriculture, veterinary medicine, and human medicine, which favors the selection of drug-resistant microbes. One of the strategies proposed to overcome the problem of AMR is to use polyvalent human immunoglobulin or IVIG. The main advantage of this classic form of passive immunization is its capacity to enhance natural immunity mechanisms to eliminate bacteria, viruses, or fungi safely and physiologically. Experimental data suggest that, for some infections, local administration of IVIG may produce better results with a lower dose than intravenous application. This review presents evidence supporting the use of polyvalent human immunoglobulin in AMR, and the potential and challenges associated with its proposed usage.

Keywords: antibiotic stewardship; antimicrobial resistance; human immunoglobulin; infection control; infectious diseases; misuse of antibiotics; public health.

Figure 1

Mechanisms of action of IVIG during the treatment of infections. The neutralization of microbes, toxins, and superantigens blocks the interaction with receptors, preventing their internalization and effects. The opsonization of distinct microbes, such as viruses, bacteria, and fungi, facilitates their phagocytosis and intracellular killing. Antibody-dependent cell-mediated cytotoxicity (ADCC) allows NK cells to kill virus-infected cells that express viral antigens on their membranes. Antibodies of IVIG may also recognize and block components of the Type III toxin secretory system of bacteria, inhibiting toxin injection into host cells. Immunoglobulin molecules in IVIG preparations scavenge activated complement fragments and, thereby, prevent indiscriminate lysis of host cells, immune damage mediated by enhanced opsonophagocytosis, and exaggerated inflammatory reaction. Created with BioRender.com.